Page 116 - Feline Cardiology

Chapter 11: Hypertrophic Cardiomyopathy 115

that impaired ventricular relaxation in people with diastolic dysfunction in people with HCM (Ohsato et al.
HCM may be influenced by a reduced afterload present 1992).
in the thick ventricle. However, when the afterload Elevated LV diastolic pressure results in elevated left
is increased in human patients with HCM, the end- atrial filling pressure and elevated pulmonary capillary
diastolic diameter and overall diastolic function is not wedge pressure (PCWP). In cats with HOCM, SAM of
increased or improved, since the viscoelastic properties the mitral valve leads to mitral regurgitation, which
of the hypertrophied ventricle remain abnormal (i.e., further elevates left atrial diastolic pressure. Left atrial
the heart was still stiff). Delayed relaxation, or regional enlargement occurs secondary to elevated left atrial
heterogeneity of relaxation due to geometric distortion pressure. The final result is transudation of plasma into
or myofiber disarray, also contribute to increased early the alveoli and development of pulmonary edema once
diastolic filling pressure (Mandinov et al. 2000). In LV diastolic pressure exceeds ∼24 mm Hg (Guyton and
people with HCM, the magnitude of regional nonuni- Lindsey 1959). Reducing LV end-diastolic volume with
formity of relaxation correlates with the severity of medical treatment (i.e., a diuretic) shifts the pressure Cardiomyopathies
global diastolic dysfunction (Bonow et al. 1987). volume loop leftward, and results in lower end-diastolic
In summary, delayed relaxation, a hallmark patho- pressure (see Figure 11.5) (Zile and Brutsaert 2002).
physiologic abnormality in HCM, may be caused by Severe LV concentric hypertrophy along with increased
abnormal calcium handling, altered LV loading, and myocardial stiffness may reduce end-diastolic volume
myocardial ischemia (see Figure 11.5). Delayed or and reduce stroke volume. Consequently, reduced renal
incomplete relaxation not only negatively impacts early perfusion activates RAAS, leading to increased circulat-
diastole, but may impair passive filling due to the con- ing blood volume and further increased diastolic filling
tinuing interaction of contractile elements and persis- pressure (Taugner 2001).
tent development of myocardial tension.
Congestive Heart Failure
Passive Diastolic Filling in HCM CHF occurs secondary to severe diastolic dysfunction in
Increased myocardial stiffness is an important compo- cats with severe HCM (see also Chapter 19). CHF occurs
nent of diastolic dysfunction in HCM. Stiffness is repre- once the PCWP exceeds approximately 24 mm Hg in
sented by the slope of the diastolic pressure-volume cats. In a retrospective study of 260 cats diagnosed with
curve (Figure 11.5). The diastolic pressure-volume HCM, 46% had CHF as evidenced by pulmonary edema
relationship is curvilinear, and pressure increases as on thoracic radiographs (Rush et al. 2002). Half of the
chamber volume increases. Myocardial hypertrophy, cats with CHF had concurrent pulmonary edema and
fibrosis, and myocyte disarray increase myocardial stiff- pleural effusion (Rush et al. 2002). The etiology of
ness, which shifts the LV end-diastolic pressure volume pleural effusion in cats with left-sided CHF is debatable.
relationship upward (see Figures 11.5, 11.6) (Mandinov Visceral pleural veins, which collect venous blood from
et al. 2000). Therefore, for any given diastolic volume, the the pleural surface of the lungs, drain into the pulmo-
diastolic pressure is greater in a stiff ventricle. Interstitial nary veins in cats. Elevated pulmonary venous pressure
fibrosis, myocyte hypertrophy, and myocyte disarray all secondary to left heart failure may lead to formation of
contribute to diastolic dysfunction, but myocyte disarray pleural effusion through elevation of hydrostatic pres-
was found to be the most important factor related to sure and transudation of plasma through the walls of

Myocardial fibrosis
Increased stiffness
Myofiber disarray
Ventricular hypertrophy
Reduced
diastolic
filling
Regional asynchrony
Abnormal calcium handling Delayed relaxation
Ischemia
Altered LV loading

Figure 11.6. Factors causing diastolic dysfunction and diastolic heart failure. Cats with HCM have diastolic dysfunction including
delayed or incomplete relaxation as well as impaired passive diastolic filling due to increased chamber stiffness. These abnormalities
lead to increased diastolic filling pressure. Congestive heart failure develops when the left ventricular end-diastolic pressure exceeds
∼24 mm Hg.